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小鼠神经母细胞瘤细胞中的热休克基因表达与细胞骨架改变

Heat shock gene expression and cytoskeletal alterations in mouse neuroblastoma cells.

作者信息

van Bergen en Henegouwen P M, Linnemans A M

出版信息

Exp Cell Res. 1987 Aug;171(2):367-75. doi: 10.1016/0014-4827(87)90169-8.

Abstract

The cytoskeleton of neuroblastoma cells, clone Neuro 2A, is altered by two stress conditions: heat shock and arsenite treatment. Microtubules are reorganized, intermediate filaments are aggregated around the nucleus, and the number of stress fibers is reduced. Since both stress modalities induce similar cytoskeletal alterations, no thermic denaturation of one or more cytoskeletal components can be involved in this process. Heat shock proteins are induced both by heat and by arsenite. However, cells treated with arsenite synthesize hsp28 which is not detected in heat-treated cells. Synthesis of all hsps is prevented by addition of actinomycin D or cycloheximide. Under these conditions no alterations are observed in the organization of microtubules and intermediate filaments during heat or arsenite treatment. However, these drugs are not able to prevent the rapid loss of stress fibers. A re-formation of the cytoskeleton during the recovery period proceeds within 3 h and is also found to occur in the presence of a protein synthesis inhibitor. These data suggest that reorganization of microtubules and intermediate filaments during a stress treatment requires the synthesis of a new protein(s), probably hsp(s).

摘要

神经母细胞瘤细胞系Neuro 2A的细胞骨架在两种应激条件下会发生改变:热休克和亚砷酸盐处理。微管会重新排列,中间丝会在细胞核周围聚集,应力纤维的数量会减少。由于这两种应激方式都会诱导相似的细胞骨架改变,因此这一过程不可能涉及一种或多种细胞骨架成分的热变性。热休克蛋白可由热和亚砷酸盐诱导产生。然而,用亚砷酸盐处理的细胞会合成hsp28,而在热休克处理的细胞中未检测到该蛋白。添加放线菌素D或环己酰亚胺可阻止所有热休克蛋白的合成。在这些条件下,热休克或亚砷酸盐处理期间微管和中间丝的组织未观察到改变。然而,这些药物无法阻止应力纤维的快速丢失。恢复期细胞骨架的重新形成在3小时内进行,并且在存在蛋白质合成抑制剂的情况下也会发生。这些数据表明,应激处理期间微管和中间丝的重新排列需要合成一种新的蛋白质,可能是热休克蛋白。

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